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- W2792395386 abstract "Genetic ablation of cyclooxygenase-2 (COX-2) in mice is known to impair fracture healing. To determine if teriparatide (human PTH1-34) can promote healing of Cox-2-deficient fractures, we performed detailed in vivo analyses using a murine stabilized tibia fracture model. Periosteal progenitor cell proliferation as well as bony callus formation was markedly reduced in Cox-2-/- mice at day 10 post-fracture. Remarkably, intermittent PTH1-34 administration increased proliferation of periosteal progenitor cells, restored callus formation on day 7, and enhanced bone formation on days 10, 14 and 21 in Cox-2-deficient mice. PTH1-34 also increased biomechanical torsional properties at days 10 or 14 in all genotypes, consistent with enhanced bony callus formation by radiologic examinations. To determine the effects of intermittent PTH1-34 for callus remodeling, TRAP staining was performed. Intermittent PTH1-34 treatment increased the number of TRAP positive cells per total callus area on day 21 in Cox-2-/- fractures. Taken together, the present findings indicate that intermittent PTH1-34 treatment could compensate for COX-2 deficiency and improve impaired fracture healing in Cox-2-deficient mice." @default.
- W2792395386 created "2018-03-29" @default.
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- W2792395386 date "2018-05-01" @default.
- W2792395386 modified "2023-10-14" @default.
- W2792395386 title "Teriparatide (human PTH1–34) compensates for impaired fracture healing in COX-2 deficient mice" @default.
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- W2792395386 doi "https://doi.org/10.1016/j.bone.2018.02.001" @default.
- W2792395386 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5878736" @default.
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